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S4 Neuro > Neuropathology > Flashcards

Neuropathology Flashcards

1
Q

The CNS is normally sterile, what are the 3 possible routes microorganisms can gain entry by?

A
  • direct spread e.g. middle ear infection, base of skull fracture (breach of barriers, entrances/ exits)
  • blood-borne e.g. sepsis, infective endocarditis
  • iatrogenic e.g. ventricular- peritoneal shunt, surgery, lumbar puncture
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2
Q

What’s one possible cause of a cerebral abscess?

A

Untreated middle ear infection

See slide 5

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3
Q

What is meningitis? Causative organisms

A

Inflammation of leptomeninges (pain/ arachnoid matter) with or without septicaemia

Neonates - E.coli
2-5yrs - H. Influenzae type B
5-30yrs- N.meningitides
>30 - s.pneumoniae

Various in immunocompromised

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4
Q

What causes the non-blanching rash sometimes seen in meningitis?

A

Septicaemia

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5
Q

What’s the most common cause of chronic meningitis? What can it lead to?

A

If untreated or immunocompromised

M. Tuberculosis

Granulomatous inflammation

Fibrosis of meninges

Nerve entrapment

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6
Q

Complications of meningitis

A

Death

Cerebral infarction (neurological deficit)

Cerebral abscess

Subdural empyema (pus in space)

Epilepsy

Systemic (septicaemia)

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7
Q

What is encephalitis? Give different sites and a common cause

A

Infection of the brain (parenchyma not meninges)

Classically viral

Neuronal cell death by virus (inclusion bodies - sites of viral replication)

Temporal lobe - herpes virus (epilepsy)

Spinal cord motor neurones - polio

Brain stem - rabies

Lymphocytic inflammatory reaction

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8
Q

What are prions? How can they cause disease?

A

Proteins (normally constituent of synapse)

Can cause problems when they mutate
- sporadic, familial, ingested

Mutated PrP interact with normal PrP to undergo a post translational conformational change -> form aggregates -> neuronal death & holes in grey matter -> spongiform encephalopathies e.g. variant Creutzfeld- Jacob disease

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9
Q

Compare variant and classic creutzfeld- Jacob disease?

A

Variant: age of death younger (28yrs), duration longer (14months), psychiatric/ behavioural symptoms, painful dyestgesiasis, delayed neurological signs, florid plaques present in large numbers, accumulation of protease- resistance prion protein

Classic: dementia, early neurological signs, Florid plaques rare, variable accumulation protease resistance prion protein

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10
Q

What is dementia? List the different types

A

Acquired global impairment of intellect, reason and personality without impairment of consciousness

  • Alzheimer’s (50%) sporadic/ familial, early (<50yrs)/ late
  • vascular dementia (20%)
  • Lewy body
  • picks disease
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11
Q

What is the pathophysiology behind Alzheimer’s?

A

Exaggerated aging process - cells take on oxidative damage, loss of cortical neurones due to increased neuronal damage by:

  • neurofibrillary tangles (intracellular twisted filaments of Tau protein which normally binds/ stabilises microtubules -> hyperphosphorylated ~ tauopathy)
  • senile plaques (foci of enlarged axons/ synaptic terminals/ dendrites. Amyloid deposition in vessels centre of plaque -> ischaemia) - ‘cotton wool lesions’ of neuronal aggregates
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12
Q

What genetic knowledge do we have on amyloid deposition and it’s role in Alzheimer’s?

A

Central to pathogenesis

-Down’s syndrome - trisomy 21 nearly all get early onset Alzheimer’s

Mutations on 3 genes on chromosome 21:

  • amyloid precursor protein gene
  • presenilin genes 1 and 2 code for components of secretase enzyme (breaks down)
  • > incomplete breakdown APP and amyloid deposited
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13
Q

What’s the normal ICP? What are the compensation mechanisms if it becomes raised?

A

0-10mmHG or 20 if coughing

Compensation:
Reduced blood volume
Reduced CSF volume
Spatial brain atrophy

Vascular mechanisms maintain cerebral blood flow as long as ICP <60mmHg

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14
Q

What can happen as a result of an expanding lesion?

A

E.g. tumour/ haemorrhage/ oedema -> raised ICP

  • Destruction of brain around lesion
  • Displacement of midline structures -> loss of symmetry (secondary injury to opp side)
  • brain shift -> internal herniation
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15
Q

What is a subfalcine herniation? Give an example

A

Same side as mass under falx cerebri

E.g cingulate gyrus pushed under falx cerebri -> compression anterior cerebral artery -> ischaemia of medial frontal/ parietal lobes/ corpus callosum

See slide 29

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16
Q

What is tentorial herniation? Give an example

A

Under tentorium cerebelli

Uncus/ medial parahippocampal gyrus through tentorial notch -> damage occulomotor nerve on same side (down and out), occlusion blood flow posterior cerebral/ superior cerebellar arteries

-> can be fatal (secondary haemorrhage into Brainstem ‘duret haemorrhage’

See slide 32

17
Q

What is a tonsilar herniation?

A

cerebellar tonsils pushes into foramen magnum compressing the Brainstem = Coning

Can eventually compress CVS centre -> reflex bradycardia = Cushings reflex

18
Q

Give examples of tumours in the the nervous system

A

Primary tumours are v rare as stable/ permanent tissue:

  • benign (meningeal origin - meningioma)
  • malignant (astrocyte origin -> astrocytoma spread along nerve tracts and through sub arachnoid space)
  • others (neurofibroma- more paediatrics, ependymoma - developing brain, neuronal - medulloblastoma)

Metastasis most common e.g. Lymphoma, renal cell carcinoma, melanoma

See slide 36/37

19
Q

What is a stroke? What are the two broad categories? Risk factors

A

Sudden event producing a disturbance of CNS function due to vascular disease (CVS disease with neurological symptoms)

  • cerebral infarction 85%
  • cerebral haemorrhage 15%

Risk factors:
Hyperlipidaemia, hypertension, diabetes mellitus

20
Q

Pathogenesis of stroke

A

Embolism (most common):
Heart - atrial fibrillation, mural thrombus
Atheromatous debris - carotid atheroma
Thrombus over ruptured atheromatous plaque
Aneurysm

Thrombosis:
Over atheromatous plaque

21
Q

Types of cerebral infarct

A

Regional - named after cerebral artery or carotid e.g. posterior circulation stroke

Lacuna - small Bvs <1cm, associated with hypertension, commonly affect basal ganglia

22
Q

Types of cerebral haemorrhage

A

Spontaneous e.g. non-traumatic

Intracerebral 10% all strokes - hypertensive vessel damage, charcot- Bouchard aneurysms, deposition amyloid around cerebral vessels in elderly, produces SOL slide 45

Subarachnoid 5% - rupture of berry aneurysms (usually bifurcation of circle of Willis) Male sex, hypertension, atheroma, links to other diseases PKD slide 48

23
Q

Symptoms of subarachnoid haemorrhage

A

Sudden severe headache - thunderclap

Sentinel headache - increasing before from small vessels

Loss of consciousness

But Usually instantly fatal

S4 Neuro (21 decks)

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